The DOI matches its Crossref record; 173 of the 173 references it cites were found in a registry or an index.
Repair of DNA Double-Strand Breaks by the Nonhomologous End Joining Pathway
Open accessAbstract
DNA double-strand breaks pose a serious threat to genome stability. In vertebrates, these breaks are predominantly repaired by nonhomologous end joining (NHEJ), which pairs DNA ends in a multiprotein synaptic complex to promote their direct ligation. NHEJ is a highly versatile pathway that uses an array of processing enzymes to modify damaged DNA ends and enable their ligation. The mechanisms of end synapsis and end processing have important implications for genome stability. Rapid and stable synapsis is necessary to limit chromosome translocations that result from the mispairing of DNA ends. Furthermore, end processing must be tightly regulated to minimize mutations at the break site. Here, we review our current mechanistic understanding of vertebrate NHEJ, with a particular focus on end synapsis and processing.
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“NHEJ operates by recognizing DSBs, processing the DNA ends, and ligating them, infrequently resulting in insertions or deletions (indels) that can disrupt gene function (Stinson & Loparo, 2021; Takata et al., 1998).”
From CRISPR/Cas9 Ribonucleoprotein Nucleofection for Genome Editing in Primary Human Keratinocytes: Knockouts, Deletions, and Homology‐Directed Repair Mutagenesis (2024) · cites this paper as Stinson & Loparo, 2021
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The mechanism of double-strand DNA break repair by the nonhomologous DNA end-joining pathway
Lieber, M. R. (2010) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.052308.093131 · Cited by 2,882
DNA Topoisomerases: Structure, Function, and Mechanism
Champoux, J. J. (2001) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.70.1.369 · Cited by 2,804
Massive genomic rearrangement acquired in a single catastrophic event during cancer development
Stephens, P. J., Greenman, C. D., Fu, B., Yang, F., Bignell, G. R., Mudie, L. J., Pleasance, E. D., Lau, K. W., Beare, D., Stebbings, L. A., et al. (2011) · Cell · doi:10.1016/j.cell.2010.11.055 · Cited by 2,414
Double-Strand Break End Resection and Repair Pathway Choice
Symington, L. S., & Gautier, J. (2011) · Annual Review of Genetics · doi:10.1146/annurev-genet-110410-132435 · Cited by 1,556
DNA double-strand break repair-pathway choice in somatic mammalian cells
Scully, R., Panday, A., Elango, R., & Willis, N. A. (2019) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-019-0152-0 · Cited by 1,542
Repair Pathway Choices and Consequences at the Double-Strand Break
Ceccaldi, R., Rondinelli, B., & D’Andrea, A. D. (2016) · Trends in Cell Biology · doi:10.1016/j.tcb.2015.07.009 · Cited by 1,499
Conserved modes of recruitment of ATM, ATR and DNA-PKcs to sites of DNA damage
Falck, J., Coates, J., & Jackson, S. P. (2005) · Nature · doi:10.1038/nature03442 · Cited by 1,304
Takata, M., Sasaki, M. S., Sonoda, E., Morrison, C., Hashimoto, M., Utsumi, H., Yamaguchi‐Iwai, Y., Shinohara, A., & Takeda, S. (1998) · The EMBO Journal · doi:10.1093/emboj/17.18.5497 · Cited by 1,229
Structure of the Ku heterodimer bound to DNA and its implications for double-strand break repair
Walker, J. R., Corpina, R. A., & Goldberg, J. D. (2001) · Nature · doi:10.1038/35088000 · Cited by 1,216
Chu, V. T., Weber, T., Wefers, B., Wurst, W., Sander, S., Rajewsky, K., & Kühn, R. (2015) · Nature Biotechnology · doi:10.1038/nbt.3198 · Cited by 1,210
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Metadata
- Authors
- Stinson, B. M., & Loparo, J. J.
- Affiliations
- Harvard University (US)
- Corresponding author
- Loparo, Joseph J.
- Venue
- Annual Review of Biochemistry
- Publisher
- Annual Reviews
- Published
- 2021-06-20
- Volume
- 90
- Issue
- 1
- Pages
- 137-164
- ISSN
- 0066-4154 (ISSN-L)
- 1545-4509
- PMC
- PMC8899865
- OpenAlex
- W3127347270
- Cited by
- 223
- References
- 173
- Citations by year
- 2026: 49 · 2025: 61 · 2024: 57 · 2023: 33 · 2022: 19 · 2021: 4
- FWCI
- 3.04
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annual Review of Biochemistry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Damon Runyon Cancer Research Foundation
- National Institutes of Health
- National Institute of General Medical Sciences (R01GM115487)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › CRISPR and Genetic Engineering
- Keywords
- non-homologous end joining, DNA double-strand breaks, DNA end processing, genome stability, chromosomal translocation, DNA ligation
- MeSH terms
- Animals, Enzymes, Humans, Models, Biological, Genomic Instability, Multiprotein Complexes, DNA Breaks, Double-Stranded, DNA End-Joining Repair, V(D)J Recombination
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